Classification and General Properties

1. Some examples of diseases caused by viruses mentioned in the tutorial include HIV, Ebola,
influenza, rabies, and smallpox.

2. The uniform classification system for viruses was established in 1971 by the International
Committee for Taxonomy of Viruses (ICTV).

3. The current virus classification system includes approximately 2,000 viruses, 6 orders, 87
families, 19 subfamilies, and 349 genera.

4. The Baltimore classification system for viruses was developed by David Baltimore.

5. The seven life cycle groups in the Baltimore classification system are based on the type of
viral genome and the process used to synthesize viral mRNA.

6. Viruses differ in terms of nucleic acid type, such as double-stranded (ds) DNA, single-
stranded (ss) DNA, dsRNA, ssRNA (+ or - strand), and retroviruses.

7. The presence or absence of an envelope in virus classification helps distinguish between

different virus types.

8. Capsid symmetry refers to the geometric arrangement of capsomers in the viral capsid.

9. Viruses cannot reproduce independently outside of living cells because they lack the cellular
machinery necessary for replication.

10. Extracellular viruses are inactive and cannot reproduce outside of living cells, while
intracellular viruses commandeer host cells for replication.

11. Viruses are vital members of the aquatic ecosystem, playing roles in nutrient cycling and
microbial population control.

12. Bacteriophages (phages) in the human gut can regulate the bacterial microbiome by
infecting and influencing bacterial populations.

13. Bacteriophages like T4 are important model organisms in virology and genetics research.

Structure of Viruses

14. A virion is a complete virus particle that consists of one or more molecules of DNA or RNA
enclosed in a protein coat (capsid).

15. The primary function of the capsid in a virus is to protect the viral genetic material and
facilitate its transfer between host cells.

16. Enveloped viruses have an outer lipid membrane in addition to their capsid, while
nonenveloped viruses lack this membrane.

17. Nonenveloped viruses have a simpler structure without the lipid envelope seen in enveloped
viruses.

18. Capsids come in various shapes, including helical, icosahedral, and complex.

19. Helical capsids are characterized by their hollow tube-like shape with self-assembling
protomers.
 20. An icosahedral capsid is a regular polyhedron with 20 equilateral faces and 12 vertices,
formed by ring or knob-shaped capsomers.

21. Some viruses have complex capsids, such as poxviruses and large bacteriophages.

Virus Replication

22. The six general steps involved in viral replication are attachment, entry, uncoating, synthesis,
assembly, and release.

23. Viral attachment to host cells occurs through ligand-receptor interactions, allowing the virus
to bind to specific host cell receptors.

24. Viruses enter host cells through fusion, endocytosis, or direct release of their genetic
material.

25. Fusion is a process in which the viral envelope fuses with the host cell's plasma membrane,
releasing the viral genome into the cell.

26. Endocytosis involves the virus being engulfed by the host cell in an endosome.

27. Uncoating of the viral genome occurs after entry into the host cell, allowing the genetic
material to become accessible.

28. DNA viruses and RNA viruses differ in how they use the host cell's machinery for synthesis
during replication.

29. Viral replication complexes enclose the machinery required for genome replication and
tightly regulate gene expression and protein synthesis.

30. Late proteins play a significant role in the assembly of new virions.

31. Virion release can occur through host cell lysis (nonenveloped viruses) or budding
(enveloped viruses).

Bacterial and Archaeal Viral Infections

32. Virulent phages immediately multiply upon entering bacterial hosts and are released by host
cell lysis.

33. Temperate phages have two reproductive options: they can reproduce lytically like virulent
phages or remain within the host cell without destroying it.

34. Lysogeny is a state in which a temperate phage's DNA integrates into the host genome,
creating a prophage.

35. Prophages are forms of the virus that remain within their host and are replicated and
inherited within the genome of progeny cells.

36. The transition from lysogeny to the lytic cycle in temperate phages is triggered by specific
conditions or signals.

37. Temperate phages can change the phenotype of their host cells, leading to immunity to
superinfection or the expression of pathogenic genes.

38. Induction is the process by which lysogenic bacteria transition to the lytic cycle, resulting in
the release of phage particles.
Infection of Eukaryotic Cells and Cancer

39. Possible outcomes of viral infections in eukaryotic host cells include cytocidal infection (cell
death), persistent infection, cytopathic effects (CPEs), and carcinogenesis.

40. Cytocidal infection results in cell death through cell lysis.

41. Persistent infections can last for years without immediate cell lysis.

42. Cytopathic effects (CPEs) are degenerative changes and abnormalities caused by viral
infections in host cells.

43. Some viruses can contribute to carcinogenesis by altering host cell regulation and promoting
the development of cancer.

44. Examples of viruses associated with human cancers include hepatitis B and C viruses, human
papillomaviruses, and Epstein-Barr virus.

45. Oncogenes are cancer-causing genes that may be activated by viruses or host cell
transformations.

46. Viruses can insert promoters or enhancers near cellular oncogenes, leading to their
abnormal activation and cancer development.

47. Surface proteins of viruses can play a crucial role in viral entry and exit from host cells.

Cultivation and Quantification of Viruses

48. Viruses cannot be cultured like cellular microorganisms due to their reliance on host cells for
replication.

49. Plaque assays are used to quantify viruses by counting the number of plaques, which
represent individual infectious units.

50. The concentration of infectious units in viral samples can be measured through plaque
assays, infectious dose assays, and lethal dose assays. These assays determine the smallest
virus amount needed to infect or kill 50% of host cells or organisms.